Atrial fibrillation (“AF”) is a cardiac arrhythmia wherein the atria beat chaotically, thereby providing generally poor conduction of blood into the ventricles of the heart and hence reducing the flow of blood throughout the body. AF has been shown to lead to long-term health problems such as increased risk of thrombolytic stroke. AF can also cause reduced cardiac efficiency, irregular ventricular rhythm and unpleasant symptoms such as palpitations and shortness of breath. In some cases, AF can trigger ventricular fibrillation (VF) wherein the ventricles of the heart beat chaotically thereby providing little or no blood flow to the brain and other organs. VF, if not terminated, is usually fatal.
Hence, it is highly desirable to terminate AF should it arise and revert the atria to a normal rhythm. The current, most common therapy for atrial fibrillation is the administration of anti-arrhythmic drugs that control atrial and ventricular rates during AF. However, these drugs can actually be proarrhythmic, causing the arrhythmia to worsen. At best, anti-arrhythmic drugs appear to provide short-term therapy. Another technique for terminating AF is to administer an electrical cardioversion shock to the atria of the heart. The cardioversion shock, if successful, terminates the chaotic pulsing of the atria and causes the atria to resume a normal beating pattern. Patients prone to AF may have an ICD implanted therein capable of detecting AF and automatically administering one or more cardioversion shocks to terminate AF. Typically, about two joules of energy is administered within each cardioversion shock at an initial voltage of between 100 to 500 volts (V). The duration of the pulse is usually between 5-15 milliseconds (ms) and is a descending voltage capacitive discharge waveform. State of the art ICDs are also capable of detecting a wide variety of other heart arrhythmias, such as VF, and for administering appropriate therapy as well. For VF, the ICD administers a much stronger cardioversion shock (referred to as a defibrillation shock) directly to the ventricles of the heart. The defibrillation shock typically has at least ten to twelve joules of electrical energy. Note that, herein, “cardioversion” generally refers to the delivery of any electrical shock intended to synchronize action potentials of myocardial cells within the heart to terminate arrhythmias. Defibrillation, herein, refers to a type of cardioversion specifically intended to terminate fibrillation.
Although atrial cardioversion shocks have been found to be effective for terminating AF within many patients, the shocks can be quite painful. One reason is that the patient is typically conscious and alert at the time the shock is administered. In contrast, the much stronger ventricular defibrillation shocks for terminating VF are typically not administered until the patient has lost consciousness and hence the patient may feel only residual chest pain upon being revived. Because AF is not usually immediately life-threatening, painful cardioversion shocks for its treatment are often perceived by patients as being worse than the condition itself and therefore not tolerated. Indeed, anxiety arising from the fear of receiving a painful cardioversion shock may be sufficient to raise the heart rate sufficiently to trigger the shock. As some patients have hundreds of AF episodes per year, techniques for reducing the pain associated with cardioversion shocks are highly desirable. It is also desirable to reduce pain associated with ventricular defibrillation shocks. Although patients receiving ventricular defibrillation shocks are usually unconscious when the shock is delivered, in some cases, such shocks are erroneously delivered while the patient is conscious due to false-positive VF detection, resulting in considerable patient pain.
One method for reducing pain arising from cardioversion shocks involves altering the stimulation waveform of the shock to, for example, reduce or smooth initial voltage peaks. See, for example, U.S. Pat. No. 5,830,236, to Mouchawar et al., entitled “System for Delivering Low Pain Therapeutic Electrical Waveforms to the Heart” and U.S. Pat. No. 5,906,633, also to Mouchawar et al., entitled “System for Delivering Rounded Low Pain Therapeutic Electrical Waveforms to the Heart.” Shock smoothing is illustrated by way of FIGS. 1 and 2. FIG. 1 illustrates a conventional cardioversion shock waveform 1 (shown in V) along with a resulting cardiac membrane response 2. Herein, the cardiac membrane response is shown in arbitrary response units for the purposes of comparison. The shock waveform is biphasic, with a peak voltage of the initial (positive) phase at about 100 V and with a peak voltage of the second (negative) phase at about 33 V. The peak of the resulting cardiac membrane response occurs at about 4 ms and is at about 50 response units. Peak voltage of the initial phase is typically regarded as the primary determinant of shock pain; whereas the peak cardiac membrane response is typically regarded as the primary indicator of shock effectiveness. Hence, with the conventional shock waveform of FIG. 1, the effectiveness of the shock is only about 50 cardiac response units; the resulting pain is associated with 100 V.
FIG. 2, in contrast, illustrates a smoothed cardioversion waveform 3 along with a resulting cardiac membrane response 4, shown in the same arbitrary response units of FIG. 1 for comparison purposes. The shock waveform of FIG. 2 is smoothed so as to reduce the peak voltage of the initial phase to about 70 V. The peak voltage of the second (negative) phase remains at about 33 V. The peak of the resulting cardiac membrane response is still about 45 response units. Hence, with the smoothed shock waveform of FIG. 2, the cardioversion shock is almost as effective as with the non-smoothed waveform of FIG. 1; whereas the resulting pain is significantly lower, i.e. the resulting pain is associated with a peak voltage of only about 70 V rather than with a peak voltage of 100 V.
One way to generate the smoothed waveform of FIG. 2 is to start with a higher initial capacitor voltage (about 160 V) than the non-smoothed waveform of FIG. 1 and then use resistive loss to lower the voltage as needed. The capacitor voltage is shown by way of phantom line 5, which decreases exponentially. The capacitor voltage at each point in time must be at least as great as the output pulse being generated at that same point in time. During times when the capacitor voltage is greater than the corresponding output shock voltage, the additional energy is dissipated as heat. Thus, pain reduction is achieved at the expense of consuming somewhat greater energy per shock.
Note that the shock waveforms of FIGS. 1 and 2 both provide a fairly substantial peak voltage for the second (negative) phase as compared to that of the initial phase. For the non-smoothed waveform of FIG. 1, the peak voltage of the second phase is at least about one third that of the initial phase. For the smoothed waveform of FIG. 2, the peak voltage of the second phase is at least about four tenths that of the initial phase. Conventionally, it is believed that the second phase must have a fairly large peak voltage is comparison with that of the initial phase to achieve a suitable defibrillation threshold. In addition, conventionally, it is believed that long duration shock phases are disadvantageous. For example, in the case of FIG. 1, the peak cardiac membrane response is achieved at about 4 ms, although the voltage remains relatively high until the 6 ms point, at which it is finally truncated. Truncation of the first phase of a conventional shock waveform is performed, in large part, to reduce the amount of shock energy delivered after the peak membrane response. In this regard, the smoothed waveform of FIG. 2 has the advantage of achieving peak membrane response just at the end of the initial phase with the voltage of the initial (positive) phase then decreasing promptly before commencement of the second (negative) phase.
Note also that the graphs of FIGS. 1 and 2, and all other graphs provided herein, include stylized representations of the parameters being illustrated. This is done so as to more clearly illustrate pertinent features of those parameters. The graphs should not be construed as illustrating actual clinically-detected parameters.
Thus, smoothed waveforms of the type shown in FIG. 2 can be effective in reducing the resulting pain. It would be desirable, however, to achieve an even greater amount of pain reduction without reducing shock effectiveness. It is to that end that certain aspects of the invention are directed. Moreover, it would also be desirable to provide a relatively simple circuit capable of generating improved shock waveforms and other aspects of the invention are directed to that end.
Another method for reducing pain arising from cardioversion shocks is to deliver a pre-pulse pain inhibition (PPI) pulse prior to the main shock. See, for example, U.S. Pat. No. 6,091,989 to Swerdlow et al., entitled “Method and Apparatus for Reduction of Pain from Electric Shock Therapies.” With PPI techniques, a relatively weak stimulus (the PPI pulse) is applied to the patient shortly before a main cardioversion shock. The human pain perception system responds to the weak stimulus in such manner that the pain associated with the subsequent main cardioversion shock is reduced or otherwise inhibited. PPI techniques typically employ either a single relatively long, low-voltage PPI pulse or a single relatively short, high-voltage PPI pulse. The long, low-voltage PPI pulse is usually delivered at about 12-20 V. The shorter, high-voltage PPI pulse is usually delivered at the voltage of the subsequent main cardioversion shock. Each has its respective advantages and disadvantages.
Conventional low-voltage and high-voltage PPI pulses are illustrated by way of the timing diagrams of FIG. 3, which show a low-voltage PPI pulse 6 followed by a high-voltage main cardioversion shock 7 and which also show a much shorter high-voltage PPI pulse 8 followed also by a main shock 9. All waveforms of FIG. 3 are monophasic, though biphasic waveforms may instead be employed. None of the waveforms has been smoothed. The exemplary low-voltage PPI pulse and its subsequent main shock are of substantially equal duration (typically about 1-10 ms) but the PPI pulse has an initial peak voltage of only about 20 V whereas the main shock has an initial peak voltage of about 100 V. The exemplary high-voltage PPI pulse is much shorter than its subsequent main shock (e.g., as short as 0.1 ms as opposed to 1-10 ms) but is of equal voltage (again about 100 V). In each case, the PPI pulse is provided to reduce the pain perceived by the patient during the subsequent main cardioversion shock. The time scale of FIG. 3 is arbitrary but, typically, PPI pulses are delivered 30-500 ms prior to the main cardioversion shock.
A significant advantage of generating a short, high-voltage PPI pulse at the same voltage as the main shock is that only a single shocking capacitor is required, precharged to the main shock voltage. To instead deliver a PPI pulse at a low-voltage followed by a main shock at a much higher voltage, two shocking capacitors are usually required—one precharged to the low-voltage and the other precharged to the high-voltage. However, high-voltage PPI pulses can be painful in and of themselves thus reducing their effectiveness in overall pain reduction. Hence, low-voltage PPI pulses are typically preferred despite the need for an extra shocking capacitor. In this regard, note that capacitors used for generating conventional pacing pulses ordinarily cannot be employed to also generate low-voltage PPI pulses, which typically require a somewhat higher voltage than the pacing pulses.
One technique for delivering high-voltage PPI pulses that are not painful in and of themselves is to utilize extremely short duration “sliver” pulses, which are typically only about 25-50 microseconds (□s) in duration. The sliver pulses are nevertheless sufficient to provide pain inhibition. Preferably, the high-voltage PPI sliver pulses are delivered between electrodes implanted within the heart, such as between a right ventricular (RV) coil and a superior vena cava (SVC) coil, so that high-voltage can be used without risk of significant pain arising from the PPI pulse itself. In particular, pain is reduced by generating the PPI pulse away from the device can or housing. Pulses instead generated using the device can as a return electrode may stimulate sensitive skin nerves and sensitive alpha motor neurons in the pectorals. The subsequent main cardioversion shock is preferably delivered using widely spaced electrodes, such as between the SVC coil and the housing of the implanted device, to ensure maximum likelihood of success. Sliver pulses are discussed in U.S. patent application Ser. No. 10/428,222 of Kroll et al., entitled “System and Method for Generating Pain Inhibition Pulses Using an Implantable Cardiac Stimulation Device”, filed Apr. 30, 2003, which is incorporated by reference herein.
Still further improvements were set forth in U.S. patent application Ser. Nos. 10/855,654 and 11/005,976, cited above. These improvements, which are also described herein-below, pertain to the use of relatively low-voltage PPI pulses with chevron-shaped waveforms and relatively high-voltage main shocks having plateau-shaped waveforms. By employing plateau-shaped waveforms for the main shocks, a greater cardiac membrane response can be achieved at an equivalent peak voltage as compared to conventional shock waveforms. As peak voltage is a significant contributor to pain caused by cardioversion shocks, the use of a plateau-shaped waveform helps achieve pain reduction without significant loss of shock effectiveness. Moreover, by employing chevron-shaped PPI pulses in combination with plateau-shaped main shocks, a relatively simple shocking circuit having a single high-voltage shocking capacitor may be used, thus eliminating the need for both low-voltage PPI capacitors and higher voltage main shock capacitors.
Although the aforementioned techniques are effective, there are still further opportunities for pain reduction. The plateau-based techniques summarized above primarily operate to reduce pain by reducing the peak voltage of the shock. For relatively short duration waveforms, this is typically sufficient. However, for longer duration waveforms—particularly waveforms having a first phase longer than 10 ms—it appears that pain receptors refire. That is, pain receptors initially triggered at the beginning of the first phase of the shock appear to refire before the first phase is complete. This results in somewhat greater perceived pain than would otherwise be expected when using a plateau-shaped waveform. The present invention is primarily directed to techniques for addressing this issue to achieve a still further reduction in pain.